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    Alomone Labs anti trka
    Altered sensory neuron differentiation in LgDel P8 CNgV. In panels A and B, single examples of wild-type (WT) and LgDel sections used for quantification presented in panels C, D and E are shown. (A) P8 CNgV had βIII-tubulin + sensory neurons (blue) in nodules separated by bundles of CN V axons that included <t>TrkB</t> + glia and axons (red, arrowheads). TrkB + neurons appeared to be a minority (see also Fig. 2 ). (B) <t>TrkA</t> + cells (green) accounted for a majority of βIII-tubulin + sensory neurons at P8. (C) P8 LgDel CNgV sensory neurons (βIII-tubulin + ) were significantly smaller, based upon distribution of diameters, than wild-type counterparts ( n =4992 neurons, wild type, 4 ganglia/4 pups/4 litters; 5675 neurons, LgDel , 5 ganglia/5 pups/4 litters; P
    Anti Trka, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti trka/product/Alomone Labs
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
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    94/100 stars

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    1) Product Images from "Selective disruption of trigeminal sensory neurogenesis and differentiation in a mouse model of 22q11.2 deletion syndrome"

    Article Title: Selective disruption of trigeminal sensory neurogenesis and differentiation in a mouse model of 22q11.2 deletion syndrome

    Journal: Disease Models & Mechanisms

    doi: 10.1242/dmm.047357

    Altered sensory neuron differentiation in LgDel P8 CNgV. In panels A and B, single examples of wild-type (WT) and LgDel sections used for quantification presented in panels C, D and E are shown. (A) P8 CNgV had βIII-tubulin + sensory neurons (blue) in nodules separated by bundles of CN V axons that included TrkB + glia and axons (red, arrowheads). TrkB + neurons appeared to be a minority (see also Fig. 2 ). (B) TrkA + cells (green) accounted for a majority of βIII-tubulin + sensory neurons at P8. (C) P8 LgDel CNgV sensory neurons (βIII-tubulin + ) were significantly smaller, based upon distribution of diameters, than wild-type counterparts ( n =4992 neurons, wild type, 4 ganglia/4 pups/4 litters; 5675 neurons, LgDel , 5 ganglia/5 pups/4 litters; P
    Figure Legend Snippet: Altered sensory neuron differentiation in LgDel P8 CNgV. In panels A and B, single examples of wild-type (WT) and LgDel sections used for quantification presented in panels C, D and E are shown. (A) P8 CNgV had βIII-tubulin + sensory neurons (blue) in nodules separated by bundles of CN V axons that included TrkB + glia and axons (red, arrowheads). TrkB + neurons appeared to be a minority (see also Fig. 2 ). (B) TrkA + cells (green) accounted for a majority of βIII-tubulin + sensory neurons at P8. (C) P8 LgDel CNgV sensory neurons (βIII-tubulin + ) were significantly smaller, based upon distribution of diameters, than wild-type counterparts ( n =4992 neurons, wild type, 4 ganglia/4 pups/4 litters; 5675 neurons, LgDel , 5 ganglia/5 pups/4 litters; P

    Techniques Used:

    Divergent progenitor regulation and sensory neuron differentiation distinguish LgDel CNgV. The left panel shows that in wild type (WT), at E9.5, there are four distinct trigeminal progenitor classes: Six1 + placode-derived (red); a novel class that are labeled by Six1 and the Wnt1 Cre lineage reporter (yellow); Wnt1 Cre + neural crest-derived (green), DAPI + (Wnt1 − ) neural crest-derived (blue hatched) and postmitotic neuroblasts (NeuN + ; gray hatched). Each class is seen at E10.5, at which time we identified symmetric and asymmetric self-renewing, as well as neurogenic modes of division among presumed neural crest progenitors. At P8, the Wnt1 Cre + subset gives rise primarily to TrkA + , Ret + and Trpv1 + presumed nociceptive neurons, and subsets of satellite and Schwann cells. We infer that the primary source of the TrkB + presumed mechanoreceptors is the Six1 + precursor population; however, current data do not definitively demonstrate this inference. The right panel shows that in LgDel , by E10.5, proportions of placode-derived cells increase and neural crest-derived cells decrease, in register with increased asymmetric neurogenic rather than self-renewing progenitor divisions of neural crest-derived cells. In parallel, neighbor relationships of each progenitor class change from equivalent in wild-type to Six1 + progenitors being more likely, and neural crest progenitors less likely, to have neighbors of the same class. These changes are accompanied by increased newly generated NeuN + neurons distributed across Six1 + , Six1 + / Wnt1 Cre + , Wnt1 Cre + or DAPI + classes. At P8, proportions of TrkA + and TrkB + sensory neurons are similar in LgDel and wild type; however, sizes are significantly smaller in LgDel . In addition, expression levels of several markers, especially those associated with nociceptors (far right), are increased. Thus, divergent proportions, neighbor relations, modes of division and neurogenesis from distinct progenitor populations prefigure divergent CNgV sensory neuron differentiation.
    Figure Legend Snippet: Divergent progenitor regulation and sensory neuron differentiation distinguish LgDel CNgV. The left panel shows that in wild type (WT), at E9.5, there are four distinct trigeminal progenitor classes: Six1 + placode-derived (red); a novel class that are labeled by Six1 and the Wnt1 Cre lineage reporter (yellow); Wnt1 Cre + neural crest-derived (green), DAPI + (Wnt1 − ) neural crest-derived (blue hatched) and postmitotic neuroblasts (NeuN + ; gray hatched). Each class is seen at E10.5, at which time we identified symmetric and asymmetric self-renewing, as well as neurogenic modes of division among presumed neural crest progenitors. At P8, the Wnt1 Cre + subset gives rise primarily to TrkA + , Ret + and Trpv1 + presumed nociceptive neurons, and subsets of satellite and Schwann cells. We infer that the primary source of the TrkB + presumed mechanoreceptors is the Six1 + precursor population; however, current data do not definitively demonstrate this inference. The right panel shows that in LgDel , by E10.5, proportions of placode-derived cells increase and neural crest-derived cells decrease, in register with increased asymmetric neurogenic rather than self-renewing progenitor divisions of neural crest-derived cells. In parallel, neighbor relationships of each progenitor class change from equivalent in wild-type to Six1 + progenitors being more likely, and neural crest progenitors less likely, to have neighbors of the same class. These changes are accompanied by increased newly generated NeuN + neurons distributed across Six1 + , Six1 + / Wnt1 Cre + , Wnt1 Cre + or DAPI + classes. At P8, proportions of TrkA + and TrkB + sensory neurons are similar in LgDel and wild type; however, sizes are significantly smaller in LgDel . In addition, expression levels of several markers, especially those associated with nociceptors (far right), are increased. Thus, divergent proportions, neighbor relations, modes of division and neurogenesis from distinct progenitor populations prefigure divergent CNgV sensory neuron differentiation.

    Techniques Used: Derivative Assay, Labeling, Generated, Expressing

    Divergent cell classes in developing and early postnatal LgDel CNgV. (A) At E9.5, Six1 + (placode), Wnt1 Cre + and DAPI + (neural crest) were seen in both genotypes. The frequency of Six + / Wnt1 Cre + cells was higher in LgDel CNgV (* P =0.0009, t -test) and the frequency of DAPI + cells was lower (* P =0.02, t -test). The arrowheads on the left indicate the location of the region enlarged in A1-A3, and those on the right indicate the location of the region enlarged in A4-A6. At E9.5, wild-type (WT) Wnt1 Cre + cells were intermixed with Six1 + cells (A1-A3), whereas Six1 + cells appeared to be differentially aggregated in LgDel (A4-A6). (B) At E10.5, Six1 + versus Wnt1 Cre + and DAPI + proportions continued to change. Asterisks indicate significant differences in LgDel (* P =0.017; Six1 + , 0.01; Wnt1 Cre + , 0.035, DAPI + ; t -test). The arrowheads on the left indicate the location of the region enlarged in B1-B3, and those on the right indicate the location of the region enlarged in B4-B6. Six1 + and Wnt1 Cre + cells in wild type appeared to be more intermixed (B1-B3), and there were local aggregates of Six1 + cells in LgDel . (C) Preservation of lineage distinctions in wild-type and LgDel P8 CNgV. Subsets of CNgV sensory neurons (gray, βIII-tubulin + ; C1) were Wnt1 Cre + (C2,C3), as were satellite glia (C3-C7). In C1-C3, the asterisks indicate locations of βIII-tubulin + sensory neurons that are not Wnt1 Cre + . In C4-C7, the asterisks indicate single Wnt1 Cre + satellite cells, and 'n' indicates the sensory neuron, labeled by βIII-tubulin in C3, of which the Wnt1 Cre + cell is a satellite. (D) Axon fascicles within P8 CNgV had subsets of Wnt1 Cre + (D1, asterisks) and Wnt1 Cre − (D2-D3) Schwann cells. (E) TrkB + presumably mechanosensory neurons (asterisks, E1,E2) were present at low frequencies in P8 wild-type and LgDel CNgV. Histograms show proportions of TrkB + (red), TrkB + / Wnt1 Cre + (red/green), Wnt1 Cre + (green) and βIII-tubulin + -only (gray) sensory neurons ( n =189 cells, wild type; 268 cells, LgDel ; 1 wild-type and 1 LgDel P8 pup). (F) TrkA + presumably nociceptive sensory neurons were Wnt1 Cre+ (green asterisks, F1,F2) and Wnt1 Cre− (red asterisks, F1,F2). Histograms show proportions of TrkA + , TrkA + / Wnt1 Cre + , Wnt1 Cre + and Wnt1 Cre − sensory neurons (βIII-tubulin) in wild type and LgDel ( n =333 cells, wild type; 279 cells, LgDel ; 1 wild-type and 1 LgDel P8 pup).
    Figure Legend Snippet: Divergent cell classes in developing and early postnatal LgDel CNgV. (A) At E9.5, Six1 + (placode), Wnt1 Cre + and DAPI + (neural crest) were seen in both genotypes. The frequency of Six + / Wnt1 Cre + cells was higher in LgDel CNgV (* P =0.0009, t -test) and the frequency of DAPI + cells was lower (* P =0.02, t -test). The arrowheads on the left indicate the location of the region enlarged in A1-A3, and those on the right indicate the location of the region enlarged in A4-A6. At E9.5, wild-type (WT) Wnt1 Cre + cells were intermixed with Six1 + cells (A1-A3), whereas Six1 + cells appeared to be differentially aggregated in LgDel (A4-A6). (B) At E10.5, Six1 + versus Wnt1 Cre + and DAPI + proportions continued to change. Asterisks indicate significant differences in LgDel (* P =0.017; Six1 + , 0.01; Wnt1 Cre + , 0.035, DAPI + ; t -test). The arrowheads on the left indicate the location of the region enlarged in B1-B3, and those on the right indicate the location of the region enlarged in B4-B6. Six1 + and Wnt1 Cre + cells in wild type appeared to be more intermixed (B1-B3), and there were local aggregates of Six1 + cells in LgDel . (C) Preservation of lineage distinctions in wild-type and LgDel P8 CNgV. Subsets of CNgV sensory neurons (gray, βIII-tubulin + ; C1) were Wnt1 Cre + (C2,C3), as were satellite glia (C3-C7). In C1-C3, the asterisks indicate locations of βIII-tubulin + sensory neurons that are not Wnt1 Cre + . In C4-C7, the asterisks indicate single Wnt1 Cre + satellite cells, and 'n' indicates the sensory neuron, labeled by βIII-tubulin in C3, of which the Wnt1 Cre + cell is a satellite. (D) Axon fascicles within P8 CNgV had subsets of Wnt1 Cre + (D1, asterisks) and Wnt1 Cre − (D2-D3) Schwann cells. (E) TrkB + presumably mechanosensory neurons (asterisks, E1,E2) were present at low frequencies in P8 wild-type and LgDel CNgV. Histograms show proportions of TrkB + (red), TrkB + / Wnt1 Cre + (red/green), Wnt1 Cre + (green) and βIII-tubulin + -only (gray) sensory neurons ( n =189 cells, wild type; 268 cells, LgDel ; 1 wild-type and 1 LgDel P8 pup). (F) TrkA + presumably nociceptive sensory neurons were Wnt1 Cre+ (green asterisks, F1,F2) and Wnt1 Cre− (red asterisks, F1,F2). Histograms show proportions of TrkA + , TrkA + / Wnt1 Cre + , Wnt1 Cre + and Wnt1 Cre − sensory neurons (βIII-tubulin) in wild type and LgDel ( n =333 cells, wild type; 279 cells, LgDel ; 1 wild-type and 1 LgDel P8 pup).

    Techniques Used: Preserving, Labeling

    2) Product Images from "Noise-induced hearing loss: neuropathic pain via Ntrk1 signaling"

    Article Title: Noise-induced hearing loss: neuropathic pain via Ntrk1 signaling

    Journal: Molecular and cellular neurosciences

    doi: 10.1016/j.mcn.2016.07.005

    Western blots and histograms depict noise-induced changes in (A) Ntrk1, (B) Slc17a6 (C) Kcnq3 and (D) Gabrg3 protein expression at 2, 14 and 28 days post-exposure. The protein bands for Ntrk1, Slc17a6, Kcnq3 and Gabrg3 protein were normalized with the
    Figure Legend Snippet: Western blots and histograms depict noise-induced changes in (A) Ntrk1, (B) Slc17a6 (C) Kcnq3 and (D) Gabrg3 protein expression at 2, 14 and 28 days post-exposure. The protein bands for Ntrk1, Slc17a6, Kcnq3 and Gabrg3 protein were normalized with the

    Techniques Used: Western Blot, Expressing

    3) Product Images from "Noise-induced hearing loss: neuropathic pain via Ntrk1 signaling"

    Article Title: Noise-induced hearing loss: neuropathic pain via Ntrk1 signaling

    Journal: Molecular and cellular neurosciences

    doi: 10.1016/j.mcn.2016.07.005

    Western blots and histograms depict noise-induced changes in (A) Ntrk1, (B) Slc17a6 (C) Kcnq3 and (D) Gabrg3 protein expression at 2, 14 and 28 days post-exposure. The protein bands for Ntrk1, Slc17a6, Kcnq3 and Gabrg3 protein were normalized with the
    Figure Legend Snippet: Western blots and histograms depict noise-induced changes in (A) Ntrk1, (B) Slc17a6 (C) Kcnq3 and (D) Gabrg3 protein expression at 2, 14 and 28 days post-exposure. The protein bands for Ntrk1, Slc17a6, Kcnq3 and Gabrg3 protein were normalized with the

    Techniques Used: Western Blot, Expressing

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    Alomone Labs anti trka
    Altered sensory neuron differentiation in LgDel P8 CNgV. In panels A and B, single examples of wild-type (WT) and LgDel sections used for quantification presented in panels C, D and E are shown. (A) P8 CNgV had βIII-tubulin + sensory neurons (blue) in nodules separated by bundles of CN V axons that included <t>TrkB</t> + glia and axons (red, arrowheads). TrkB + neurons appeared to be a minority (see also Fig. 2 ). (B) <t>TrkA</t> + cells (green) accounted for a majority of βIII-tubulin + sensory neurons at P8. (C) P8 LgDel CNgV sensory neurons (βIII-tubulin + ) were significantly smaller, based upon distribution of diameters, than wild-type counterparts ( n =4992 neurons, wild type, 4 ganglia/4 pups/4 litters; 5675 neurons, LgDel , 5 ganglia/5 pups/4 litters; P
    Anti Trka, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti trka/product/Alomone Labs
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    anti trka - by Bioz Stars, 2022-07
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    Alomone Labs atto 633 labeled anti trka antibody anti trka extracellular atto 633
    Single-step photobleaching of <t>Atto-633</t> anti-TrkA and Atto-488 anti-p75 NTR . Intensity profiles of a single Atto-633-labeled TrkA (A) and Atto-488-labeled p75 NTR (B) signal. Histograms show the intensity value of every spot for TrkA (C) and p75 NTR (D) in a recording superimposed with a single-fitted Gaussian curve (blue line).
    Atto 633 Labeled Anti Trka Antibody Anti Trka Extracellular Atto 633, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Altered sensory neuron differentiation in LgDel P8 CNgV. In panels A and B, single examples of wild-type (WT) and LgDel sections used for quantification presented in panels C, D and E are shown. (A) P8 CNgV had βIII-tubulin + sensory neurons (blue) in nodules separated by bundles of CN V axons that included TrkB + glia and axons (red, arrowheads). TrkB + neurons appeared to be a minority (see also Fig. 2 ). (B) TrkA + cells (green) accounted for a majority of βIII-tubulin + sensory neurons at P8. (C) P8 LgDel CNgV sensory neurons (βIII-tubulin + ) were significantly smaller, based upon distribution of diameters, than wild-type counterparts ( n =4992 neurons, wild type, 4 ganglia/4 pups/4 litters; 5675 neurons, LgDel , 5 ganglia/5 pups/4 litters; P

    Journal: Disease Models & Mechanisms

    Article Title: Selective disruption of trigeminal sensory neurogenesis and differentiation in a mouse model of 22q11.2 deletion syndrome

    doi: 10.1242/dmm.047357

    Figure Lengend Snippet: Altered sensory neuron differentiation in LgDel P8 CNgV. In panels A and B, single examples of wild-type (WT) and LgDel sections used for quantification presented in panels C, D and E are shown. (A) P8 CNgV had βIII-tubulin + sensory neurons (blue) in nodules separated by bundles of CN V axons that included TrkB + glia and axons (red, arrowheads). TrkB + neurons appeared to be a minority (see also Fig. 2 ). (B) TrkA + cells (green) accounted for a majority of βIII-tubulin + sensory neurons at P8. (C) P8 LgDel CNgV sensory neurons (βIII-tubulin + ) were significantly smaller, based upon distribution of diameters, than wild-type counterparts ( n =4992 neurons, wild type, 4 ganglia/4 pups/4 litters; 5675 neurons, LgDel , 5 ganglia/5 pups/4 litters; P

    Article Snippet: The primary antibodies used were mouse anti-βIII tubulin (BioLegend, 801201, 1:1000), rabbit anti-Six1 (Proteintech, 10709, 1:1500), rabbit anti-fibronectin (Millipore, AB2033, 1:1000), anti-cleaved caspase 3 (Cell Signaling Technology, 9661, 1:200), chicken anti-GFP (Abcam, ab13970, 1:1000), mouse anti-NeuN (Merck Millipore, MAB377, 1:1000), rabbit anti-NeuN (Cell Signaling Technology, 24307, 1:400), mouse anti-BrdU (BD Biosciences, 555627, 1:100), rat anti-BrdU (Novus, NB500-169, 1:100), rabbit anti-Sox2 (Stemgent, 09-0024, 1:100), goat anti-TrkB (R & D Systems, AF1494, 1:100), anti-TrkA (Alomone Labs, ANT-018, 1:100), goat anti-Ret (Neuromics, GT15002, 1:50) and rabbit anti-TrpV1 (Alomone Labs, ACC-030, 1:100).

    Techniques:

    Divergent progenitor regulation and sensory neuron differentiation distinguish LgDel CNgV. The left panel shows that in wild type (WT), at E9.5, there are four distinct trigeminal progenitor classes: Six1 + placode-derived (red); a novel class that are labeled by Six1 and the Wnt1 Cre lineage reporter (yellow); Wnt1 Cre + neural crest-derived (green), DAPI + (Wnt1 − ) neural crest-derived (blue hatched) and postmitotic neuroblasts (NeuN + ; gray hatched). Each class is seen at E10.5, at which time we identified symmetric and asymmetric self-renewing, as well as neurogenic modes of division among presumed neural crest progenitors. At P8, the Wnt1 Cre + subset gives rise primarily to TrkA + , Ret + and Trpv1 + presumed nociceptive neurons, and subsets of satellite and Schwann cells. We infer that the primary source of the TrkB + presumed mechanoreceptors is the Six1 + precursor population; however, current data do not definitively demonstrate this inference. The right panel shows that in LgDel , by E10.5, proportions of placode-derived cells increase and neural crest-derived cells decrease, in register with increased asymmetric neurogenic rather than self-renewing progenitor divisions of neural crest-derived cells. In parallel, neighbor relationships of each progenitor class change from equivalent in wild-type to Six1 + progenitors being more likely, and neural crest progenitors less likely, to have neighbors of the same class. These changes are accompanied by increased newly generated NeuN + neurons distributed across Six1 + , Six1 + / Wnt1 Cre + , Wnt1 Cre + or DAPI + classes. At P8, proportions of TrkA + and TrkB + sensory neurons are similar in LgDel and wild type; however, sizes are significantly smaller in LgDel . In addition, expression levels of several markers, especially those associated with nociceptors (far right), are increased. Thus, divergent proportions, neighbor relations, modes of division and neurogenesis from distinct progenitor populations prefigure divergent CNgV sensory neuron differentiation.

    Journal: Disease Models & Mechanisms

    Article Title: Selective disruption of trigeminal sensory neurogenesis and differentiation in a mouse model of 22q11.2 deletion syndrome

    doi: 10.1242/dmm.047357

    Figure Lengend Snippet: Divergent progenitor regulation and sensory neuron differentiation distinguish LgDel CNgV. The left panel shows that in wild type (WT), at E9.5, there are four distinct trigeminal progenitor classes: Six1 + placode-derived (red); a novel class that are labeled by Six1 and the Wnt1 Cre lineage reporter (yellow); Wnt1 Cre + neural crest-derived (green), DAPI + (Wnt1 − ) neural crest-derived (blue hatched) and postmitotic neuroblasts (NeuN + ; gray hatched). Each class is seen at E10.5, at which time we identified symmetric and asymmetric self-renewing, as well as neurogenic modes of division among presumed neural crest progenitors. At P8, the Wnt1 Cre + subset gives rise primarily to TrkA + , Ret + and Trpv1 + presumed nociceptive neurons, and subsets of satellite and Schwann cells. We infer that the primary source of the TrkB + presumed mechanoreceptors is the Six1 + precursor population; however, current data do not definitively demonstrate this inference. The right panel shows that in LgDel , by E10.5, proportions of placode-derived cells increase and neural crest-derived cells decrease, in register with increased asymmetric neurogenic rather than self-renewing progenitor divisions of neural crest-derived cells. In parallel, neighbor relationships of each progenitor class change from equivalent in wild-type to Six1 + progenitors being more likely, and neural crest progenitors less likely, to have neighbors of the same class. These changes are accompanied by increased newly generated NeuN + neurons distributed across Six1 + , Six1 + / Wnt1 Cre + , Wnt1 Cre + or DAPI + classes. At P8, proportions of TrkA + and TrkB + sensory neurons are similar in LgDel and wild type; however, sizes are significantly smaller in LgDel . In addition, expression levels of several markers, especially those associated with nociceptors (far right), are increased. Thus, divergent proportions, neighbor relations, modes of division and neurogenesis from distinct progenitor populations prefigure divergent CNgV sensory neuron differentiation.

    Article Snippet: The primary antibodies used were mouse anti-βIII tubulin (BioLegend, 801201, 1:1000), rabbit anti-Six1 (Proteintech, 10709, 1:1500), rabbit anti-fibronectin (Millipore, AB2033, 1:1000), anti-cleaved caspase 3 (Cell Signaling Technology, 9661, 1:200), chicken anti-GFP (Abcam, ab13970, 1:1000), mouse anti-NeuN (Merck Millipore, MAB377, 1:1000), rabbit anti-NeuN (Cell Signaling Technology, 24307, 1:400), mouse anti-BrdU (BD Biosciences, 555627, 1:100), rat anti-BrdU (Novus, NB500-169, 1:100), rabbit anti-Sox2 (Stemgent, 09-0024, 1:100), goat anti-TrkB (R & D Systems, AF1494, 1:100), anti-TrkA (Alomone Labs, ANT-018, 1:100), goat anti-Ret (Neuromics, GT15002, 1:50) and rabbit anti-TrpV1 (Alomone Labs, ACC-030, 1:100).

    Techniques: Derivative Assay, Labeling, Generated, Expressing

    Divergent cell classes in developing and early postnatal LgDel CNgV. (A) At E9.5, Six1 + (placode), Wnt1 Cre + and DAPI + (neural crest) were seen in both genotypes. The frequency of Six + / Wnt1 Cre + cells was higher in LgDel CNgV (* P =0.0009, t -test) and the frequency of DAPI + cells was lower (* P =0.02, t -test). The arrowheads on the left indicate the location of the region enlarged in A1-A3, and those on the right indicate the location of the region enlarged in A4-A6. At E9.5, wild-type (WT) Wnt1 Cre + cells were intermixed with Six1 + cells (A1-A3), whereas Six1 + cells appeared to be differentially aggregated in LgDel (A4-A6). (B) At E10.5, Six1 + versus Wnt1 Cre + and DAPI + proportions continued to change. Asterisks indicate significant differences in LgDel (* P =0.017; Six1 + , 0.01; Wnt1 Cre + , 0.035, DAPI + ; t -test). The arrowheads on the left indicate the location of the region enlarged in B1-B3, and those on the right indicate the location of the region enlarged in B4-B6. Six1 + and Wnt1 Cre + cells in wild type appeared to be more intermixed (B1-B3), and there were local aggregates of Six1 + cells in LgDel . (C) Preservation of lineage distinctions in wild-type and LgDel P8 CNgV. Subsets of CNgV sensory neurons (gray, βIII-tubulin + ; C1) were Wnt1 Cre + (C2,C3), as were satellite glia (C3-C7). In C1-C3, the asterisks indicate locations of βIII-tubulin + sensory neurons that are not Wnt1 Cre + . In C4-C7, the asterisks indicate single Wnt1 Cre + satellite cells, and 'n' indicates the sensory neuron, labeled by βIII-tubulin in C3, of which the Wnt1 Cre + cell is a satellite. (D) Axon fascicles within P8 CNgV had subsets of Wnt1 Cre + (D1, asterisks) and Wnt1 Cre − (D2-D3) Schwann cells. (E) TrkB + presumably mechanosensory neurons (asterisks, E1,E2) were present at low frequencies in P8 wild-type and LgDel CNgV. Histograms show proportions of TrkB + (red), TrkB + / Wnt1 Cre + (red/green), Wnt1 Cre + (green) and βIII-tubulin + -only (gray) sensory neurons ( n =189 cells, wild type; 268 cells, LgDel ; 1 wild-type and 1 LgDel P8 pup). (F) TrkA + presumably nociceptive sensory neurons were Wnt1 Cre+ (green asterisks, F1,F2) and Wnt1 Cre− (red asterisks, F1,F2). Histograms show proportions of TrkA + , TrkA + / Wnt1 Cre + , Wnt1 Cre + and Wnt1 Cre − sensory neurons (βIII-tubulin) in wild type and LgDel ( n =333 cells, wild type; 279 cells, LgDel ; 1 wild-type and 1 LgDel P8 pup).

    Journal: Disease Models & Mechanisms

    Article Title: Selective disruption of trigeminal sensory neurogenesis and differentiation in a mouse model of 22q11.2 deletion syndrome

    doi: 10.1242/dmm.047357

    Figure Lengend Snippet: Divergent cell classes in developing and early postnatal LgDel CNgV. (A) At E9.5, Six1 + (placode), Wnt1 Cre + and DAPI + (neural crest) were seen in both genotypes. The frequency of Six + / Wnt1 Cre + cells was higher in LgDel CNgV (* P =0.0009, t -test) and the frequency of DAPI + cells was lower (* P =0.02, t -test). The arrowheads on the left indicate the location of the region enlarged in A1-A3, and those on the right indicate the location of the region enlarged in A4-A6. At E9.5, wild-type (WT) Wnt1 Cre + cells were intermixed with Six1 + cells (A1-A3), whereas Six1 + cells appeared to be differentially aggregated in LgDel (A4-A6). (B) At E10.5, Six1 + versus Wnt1 Cre + and DAPI + proportions continued to change. Asterisks indicate significant differences in LgDel (* P =0.017; Six1 + , 0.01; Wnt1 Cre + , 0.035, DAPI + ; t -test). The arrowheads on the left indicate the location of the region enlarged in B1-B3, and those on the right indicate the location of the region enlarged in B4-B6. Six1 + and Wnt1 Cre + cells in wild type appeared to be more intermixed (B1-B3), and there were local aggregates of Six1 + cells in LgDel . (C) Preservation of lineage distinctions in wild-type and LgDel P8 CNgV. Subsets of CNgV sensory neurons (gray, βIII-tubulin + ; C1) were Wnt1 Cre + (C2,C3), as were satellite glia (C3-C7). In C1-C3, the asterisks indicate locations of βIII-tubulin + sensory neurons that are not Wnt1 Cre + . In C4-C7, the asterisks indicate single Wnt1 Cre + satellite cells, and 'n' indicates the sensory neuron, labeled by βIII-tubulin in C3, of which the Wnt1 Cre + cell is a satellite. (D) Axon fascicles within P8 CNgV had subsets of Wnt1 Cre + (D1, asterisks) and Wnt1 Cre − (D2-D3) Schwann cells. (E) TrkB + presumably mechanosensory neurons (asterisks, E1,E2) were present at low frequencies in P8 wild-type and LgDel CNgV. Histograms show proportions of TrkB + (red), TrkB + / Wnt1 Cre + (red/green), Wnt1 Cre + (green) and βIII-tubulin + -only (gray) sensory neurons ( n =189 cells, wild type; 268 cells, LgDel ; 1 wild-type and 1 LgDel P8 pup). (F) TrkA + presumably nociceptive sensory neurons were Wnt1 Cre+ (green asterisks, F1,F2) and Wnt1 Cre− (red asterisks, F1,F2). Histograms show proportions of TrkA + , TrkA + / Wnt1 Cre + , Wnt1 Cre + and Wnt1 Cre − sensory neurons (βIII-tubulin) in wild type and LgDel ( n =333 cells, wild type; 279 cells, LgDel ; 1 wild-type and 1 LgDel P8 pup).

    Article Snippet: The primary antibodies used were mouse anti-βIII tubulin (BioLegend, 801201, 1:1000), rabbit anti-Six1 (Proteintech, 10709, 1:1500), rabbit anti-fibronectin (Millipore, AB2033, 1:1000), anti-cleaved caspase 3 (Cell Signaling Technology, 9661, 1:200), chicken anti-GFP (Abcam, ab13970, 1:1000), mouse anti-NeuN (Merck Millipore, MAB377, 1:1000), rabbit anti-NeuN (Cell Signaling Technology, 24307, 1:400), mouse anti-BrdU (BD Biosciences, 555627, 1:100), rat anti-BrdU (Novus, NB500-169, 1:100), rabbit anti-Sox2 (Stemgent, 09-0024, 1:100), goat anti-TrkB (R & D Systems, AF1494, 1:100), anti-TrkA (Alomone Labs, ANT-018, 1:100), goat anti-Ret (Neuromics, GT15002, 1:50) and rabbit anti-TrpV1 (Alomone Labs, ACC-030, 1:100).

    Techniques: Preserving, Labeling

    Western blots and histograms depict noise-induced changes in (A) Ntrk1, (B) Slc17a6 (C) Kcnq3 and (D) Gabrg3 protein expression at 2, 14 and 28 days post-exposure. The protein bands for Ntrk1, Slc17a6, Kcnq3 and Gabrg3 protein were normalized with the

    Journal: Molecular and cellular neurosciences

    Article Title: Noise-induced hearing loss: neuropathic pain via Ntrk1 signaling

    doi: 10.1016/j.mcn.2016.07.005

    Figure Lengend Snippet: Western blots and histograms depict noise-induced changes in (A) Ntrk1, (B) Slc17a6 (C) Kcnq3 and (D) Gabrg3 protein expression at 2, 14 and 28 days post-exposure. The protein bands for Ntrk1, Slc17a6, Kcnq3 and Gabrg3 protein were normalized with the

    Article Snippet: The membrane was incubated overnight with 1:200 rabbit anti-Ntrk1 (Alomone Labs, Jerusalem, Israel), 1:5000 mouse anti-Slc17a6 (cat no. MAB5504; EMD Millipore, USA), 1:1000 rabbit polyclonal anti-Kcnq3 (cat no. NBP1-46666; Novus Biologicals, USA) or 1:5000 rabbit anti-actin (cat no; MAB1501; EMD Millipore, USA.) at 4 °C, followed by a 2-hr incubation with appropriate hydrogen peroxidase conjugated secondary antibody (Pierce Chemical Co., Rockford, IL).

    Techniques: Western Blot, Expressing

    Single-step photobleaching of Atto-633 anti-TrkA and Atto-488 anti-p75 NTR . Intensity profiles of a single Atto-633-labeled TrkA (A) and Atto-488-labeled p75 NTR (B) signal. Histograms show the intensity value of every spot for TrkA (C) and p75 NTR (D) in a recording superimposed with a single-fitted Gaussian curve (blue line).

    Journal: bioRxiv

    Article Title: Live cell imaging of single neurotrophin receptor molecules on human neuron in Alzheimer’s disease

    doi: 10.1101/2020.02.17.953174

    Figure Lengend Snippet: Single-step photobleaching of Atto-633 anti-TrkA and Atto-488 anti-p75 NTR . Intensity profiles of a single Atto-633-labeled TrkA (A) and Atto-488-labeled p75 NTR (B) signal. Histograms show the intensity value of every spot for TrkA (C) and p75 NTR (D) in a recording superimposed with a single-fitted Gaussian curve (blue line).

    Article Snippet: Neurons were incubated with Atto-633 labeled anti-TrkA antibody (anti-TrkA (extracellular)-Atto-633, 1:100, Alomone Labs) or Atto-488 labeled anti-p75NTR antibody (anti-p75NTR (extracellular)-Atto-488,1:100, Alomone Labs) for 6 minutes at 37°C.

    Techniques: Labeling